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Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during systole. Common causes include mitral valve prolapse, ischemic papillary muscle dysfunction, rheumatic fever, and annular dilation secondary to LV systolic dysfunction and dilation. Complications include progressive heart failure, arrhythmias, and endocarditis. Symptoms and signs include palpitations, dyspnea, and a holosystolic apical murmur. Diagnosis is by physical examination and echocardiography. Prognosis depends on LV function and severity and duration of MR. Patients with mild, asymptomatic MR may be monitored, but progressive or symptomatic MR requires mitral valve repair or replacement.
Etiology
MR may be acute or chronic. Causes of acute MR include ischemic papillary muscle dysfunction or rupture; infective endocarditis; acute rheumatic fever; spontaneous, traumatic, or ischemic tears or rupture of the mitral valve leaflets or subvalvular apparatus; acute dilation of the LV due to myocarditis or ischemia; and mechanical failure of a prosthetic mitral valve.
Common causes of chronic MR include those of acute MR plus myxomatous degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse (MVP), mitral annular enlargement, and nonischemic papillary muscle dysfunction (eg, due to LV enlargement). Uncommon causes of chronic MR include a congenital endocardial cushion defect with a cleft anterior leaflet, SLE, acromegaly, myxoma involving the valve or chordae, and calcification of the mitral annulus (mainly in elderly women).
In infants, the most likely causes of MR are papillary muscle dysfunction, endocardial fibroelastosis, acute myocarditis, cleft mitral valve with or without an endocardial cushion defect, and myxomatous degeneration of the mitral valve. MR may coexist with mitral stenosis when thickened valvular leaflets do not close.
Pathophysiology
Acute MR may cause acute pulmonary edema and biventricular failure with cardiogenic shock or sudden cardiac death. Complications of chronic MR include gradual enlargement of the left atrium (LA); LV enlargement and hypertrophy, which initially compensates for regurgitant flow (preserving forward stroke volume) but eventually decompensates (reducing forward stroke volume); atrial fibrillation (AF), which may be further complicated by thromboembolism; and infective endocarditis.
Symptoms and Signs
Acute MR causes the same symptoms and signs as acute heart failure and cardiogenic shock (see Coronary Artery Disease: Hypotension and cardiogenic shock). Most patients with chronic MR are initially asymptomatic and develop symptoms insidiously as the LA enlarges, pulmonary artery and venous pressure increases, and LV remodeling occurs. Symptoms include dyspnea, fatigue (due to heart failure), orthopnea, and palpitations (often due to AF). Rarely, patients present with endocarditis (eg, fever, weight loss, embolic phenomena).
Signs develop only when MR becomes moderate to severe. Inspection and palpation may detect a brisk apical impulse and sustained left parasternal movement due to systolic expansion of an enlarged LA. An LV impulse that is sustained, enlarged, and displaced downward and to the left suggests LV hypertrophy and dilation. A diffuse precordial lift occurs with severe MR because the LA enlarges, causing anterior cardiac displacement, and pulmonary hypertension causes right ventricular hypertrophy. A regurgitant murmur (or thrill) may also be palpable in severe cases.
On auscultation, the 1st heart sound (S1) may be soft (or occasionally loud). A 3rd heart sound (S3) at the apex reflects a dilated LV and important MR.
The cardinal sign of MR is a holosystolic (pansystolic) murmur, heard best at the apex with the diaphragm of the stethoscope when the patient is in the left lateral decubitus position. In mild MR, the systolic murmur may be abbreviated or occur late in systole. The murmur begins with S1 in conditions causing leaflet incompetency throughout systole, but it often begins after S1 (eg, when chamber dilation during systole distorts the valve apparatus or when myocardial ischemia or fibrosis alters dynamics). When the murmur begins after S1, it always continues to the 2nd heart sound (S2). The murmur radiates toward the left axilla; intensity may remain the same or vary. If intensity varies, the murmur tends to crescendo in volume up to S2. MR murmurs increase in intensity with handgrip or squatting because peripheral vascular resistance to ventricular ejection increases, augmenting regurgitation into the LA; murmurs decrease in intensity with standing or the Valsalva maneuver. A short rumbling mid-diastolic inflow murmur due to torrential mitral diastolic flow may be heard following an S3 . In patients with posterior leaflet prolapse, the murmur may be coarse and radiate to the upper sternum, mimicking aortic stenosis.
MR murmurs may be confused with tricuspid regurgitation, which can be distinguished because its murmur is augmented during inspiration.
Diagnosis
Diagnosis is suspected clinically and confirmed by echocardiography. Doppler echocardiography is used to detect regurgitant flow and help quantify its severity; 2-dimensional or 3-dimensional echocardiography is used to determine the cause of MR and to detect pulmonary hypertension.
If endocarditis or valvular thrombi are suspected, transesophageal echocardiography (TEE) can provide a more detailed view of the mitral valve and LA. TEE is also indicated when mitral valve repair instead of replacement is being considered to confirm the anatomy in more detail.
An ECG and chest x-ray are usually obtained initially. ECG may show LA enlargement and LV hypertrophy with or without ischemia. Sinus rhythm is usually present when MR is acute because the atria have not had time to stretch and remodel.
Chest x-ray in acute MR may show pulmonary edema; abnormalities in cardiac silhouette are not evident unless an underlying chronic disorder is also present. Chest x-ray in chronic MR may show LA and LV enlargement. It may also show pulmonary vascular congestion and pulmonary edema with heart failure.
Cardiac catheterization is done before surgery, mainly to determine whether coronary artery disease (CAD) is present. A prominent systolic c-v wave is seen on pulmonary artery occlusion pressure (pulmonary capillary wedge pressure) tracings during ventricular systole. Ventriculography can be used to quantify MR. Cardiac MRI can accurately measure regurgitant fraction and determine the underlying cause of dilated myopathy with MR.
Prognosis
Prognosis varies by acuity and cause of MR. Once MR becomes severe, about 10% of asymptomatic patients become symptomatic per year thereafter. About 10% of patients with chronic MR caused by MVP require surgical intervention.
Treatment
Acute MR requires emergency mitral valve repair or replacement; patients with ischemic papillary muscle rupture may also require coronary revascularization. Pending surgery, nitroprusside or nitroglycerin infusion may be used to reduce afterload, thus improving forward stroke volume and reducing ventricular and regurgitant volume.
Definitive treatment of chronic MR is also mitral valve repair or replacement, but patients with asymptomatic or mild chronic MR and no pulmonary hypertension or AF may do well with periodic monitoring. ACE inhibitors or angiotensin II receptor blockers are used to decrease left ventricular preload and afterload. They are used in patients with moderate mitral insufficiency to delay dilation of the LV. Loop diuretics such as furosemide are helpful in patients with exertional or nocturnal dyspnea. Digoxin may reduce symptoms in patients with AF or those in whom valve surgery is not appropriate. The ideal timing for surgery is uncertain, but intervention before ventricular decompensation (defined as echocardiographic end-diastolic dimension > 70 mm, end-systolic dimension > 45 mm, and ejection fraction < 60%) improves outcomes and decreases the chance of worsening LV function. After decompensation, ventricular function becomes dependent on the afterload reduction of MR, and in about 50% of decompensated patients, valve replacement causes a markedly depressed ejection fraction. For patients with moderate MR and significant CAD, perioperative mortality rate is 1.5% with bypass surgery alone and 25% with concomitant valve replacement. If technically feasible, valve repair instead of replacement is preferred; perioperative mortality rate is 2 to 4% (compared with 5 to 10% for replacement), and long-term prognosis is good (80 to 94% survival rate at 5 to 10 yr, compared with 40 to 60% for replacement).
New percutaneous procedures that tailor the mitral leaflets have been used in eldely and high-risk patients, and percutaneous placement of artificial valves is under trial.
Antibiotic prophylaxis is no longer recommended except for patients who have had valve replacement (see Table 4: Endocarditis: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures* ).
Anticoagulants are used to prevent thromboemboli (see Pulmonary Embolism: Prevention) in patients with heart failure or AF. Although severe MR without mitral stenosis or AF is less likely to be complicated by atrial thrombosis, most cardiologists still recommend anticoagulants.
Last full review/revision March 2007 by Paul H. Tanser, MD
Content last modified June 2010
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